Exploring the mystery of tumor metabolism: Warburg effect and mitochondrial metabolism fighting side by side.

The metabolic reconfiguration of tumor cells constitutes a pivotal aspect of tumor proliferation and advancement. This study delves into two primary facets of tumor metabolism: the Warburg effect and mitochondrial metabolism, elucidating their contributions to tumor dominance. The Warburg effect facilitates efficient energy acquisition by tumor cells through aerobic glycolysis and lactic acid fermentation, offering metabolic advantages conducive to growth and proliferation. Simultaneously, mitochondrial metabolism, serving as the linchpin of sustained tumor vitality, orchestrates the tricarboxylic acid cycle and electron transport chain, furnishing a steadfast and dependable wellspring of biosynthesis for tumor cells. Regarding targeted therapy, this discourse examines extant strategies targeting tumor glycolysis and mitochondrial metabolism, underscoring their potential efficacy in modulating tumor metabolism while envisaging future research trajectories and treatment paradigms in the realm of tumor metabolism. By means of a thorough exploration of tumor metabolism, this study aspires to furnish crucial insights into the regulation of tumor metabolic processes, thereby furnishing valuable guidance for the development of novel therapeutic modalities. This comprehensive deliberation is poised to catalyze advancements in tumor metabolism research and offer novel perspectives and pathways for the formulation of cancer treatment strategies in the times ahead.

Ferroptosis: a new hunter of hepatocellular carcinoma.

Ferroptosis is an iron ion-dependent, regulatory cell death modality driven by intracellular lipid peroxidation that plays a key role in the development of HCC. Studies have shown that various clinical agents (e.g., sorafenib) have ferroptosis inducer-like effects and can exert therapeutic effects by modulating different key factors in the ferroptosis pathway. This implies that targeting tumor cell ferroptosis may be a very promising strategy for tumor therapy. In this paper, we summarize the prerequisites and defense systems for the occurrence of ferroptosis and the regulatory targets of drug-mediated ferroptosis action in HCC, the differences and connections between ferroptosis and other programmed cell deaths. We aim to summarize the theoretical basis, classical inducers of ferroptosis and research progress of ferroptosis in HCC cells, clued to the treatment of HCC by regulating ferroptosis network. Further investigation of the specific mechanisms of ferroptosis and the development of hepatocellular carcinoma and interventions at different stages of hepatocellular carcinoma will help us to deepen our understanding of hepatocellular carcinoma, with a view to providing new and more precise preventive as well as therapeutic measures for patients.

Gene expression profile of the Gs-coupled prostacyclin receptor in human vascular smooth muscle cells.

Migration and proliferation of medial smooth muscle cells (SMC) in the arterial intima contributes to the development of atherosclerotic plaques and restenotic processes after coronary angioplasty. Prostacyclin (PGI2)-mediated stimulation of cyclic adenosine 3'5'-monophosphate (cAMP) signaling is believed to be important for maintaining SMC in a quiescent state. In order to identify new cellular targets of PGI2/cAMP action, we have used microarray screening to examine changes in the transcriptional profile in human vascular SMC in response to exposure to the stable PGI2 mimetic iloprost. We have identified 83 genes with significantly altered expression after iloprost (100 nM) exposure for 6 hr. Fifty-one genes were upregulated, among them stanniocalcin precursor (18.8+/-2.7), zinc finger transcription factor (7.8+/-2.0), hyaluronan synthase 2 (6.8+/-1.8), cyclooxygenase 2 (4.7+/-0.8), dual specific phosphatase (3.9+/-0.5) and vascular endothelial growth factor (2.3+/-0.4). Thirty-two genes were reduced, among them cystein-rich angiogenic protein (-14.9+/-1.3), monocyte chemotactic protein 1 (-7.4+/-1.1) and plasminogen activator inhibitor PAI-1 (-4.5+/-0.5). By means of semi-quantitative RT-PCR, time-courses of gene expression were established. The present study identified genes not hitherto recognized to be targets of PGI2 action, providing further insight into its cAMP-mediated effects on SMC growth, migration and matrix secretion.